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dc.contributor.author
Fiore, M. C.  
dc.contributor.author
Jimenez, P. M.  
dc.contributor.author
Cremonezzi, D.  
dc.contributor.author
Juncos, L. I.  
dc.contributor.author
Garcia, Nestor Horacio  
dc.date.available
2023-03-16T13:03:42Z  
dc.date.issued
2011-05  
dc.identifier.citation
Fiore, M. C.; Jimenez, P. M.; Cremonezzi, D.; Juncos, L. I.; Garcia, Nestor Horacio; Statins reverse renal inflammation and endothelial dysfunction induced by chronic high salt intake; American Physiological Society; American Journal Of Physiology-renal Physiology; 301; 2; 5-2011; 263-270  
dc.identifier.issn
1931-857X  
dc.identifier.uri
http://hdl.handle.net/11336/190748  
dc.description.abstract
High salt intake (HS) is a risk factor for cardiovascular and kidney disease. Indeed, HS may promote blood-pressure-independent tissue injury via inflammatory factors. The lipid-lowering 3-hydroxy 3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors exert beneficial lipid-independent effects, reducing the expression and synthesis of inflammatory factors. We hypothesized that HS impairs kidney structure and function in the absence of hypertension, and these changes are reversed by atorvastatin. Four groups of rats were treated for 6 wk in metabolic cages with their diets: normal salt (NS); HS, NS plus atorvastatin and HS plus atorvastatin. We measured basal and final body weight, urinary sodium and protein excretion (UProtV), and systolic blood pressure (SBP). At the end of the experimental period, cholesterolemia, creatinine clearance, renal vascular reactivity, glomerular volume, cortical and glomerular endothelial nitric oxide synthase (eNOS), and transforming growth factor (TGF)-β expression were measured. We found no differences in SBP, body weight, and cholesterolemia. HS rats had increased creatinine clearence, UProtV, and glomerular volume at the end of the study. Acetyl-choline-induced vasodilatation decreased by 40.4% in HS rats (P < 0.05). HS decreased cortical and glomerular eNOS and caused mild glomerular sclerosis, interstitial mononuclear cell infiltration, and increased cortical expression of TGF-β. All of these salt-induced changes were reversed by atorvastatin. We conclude that long-term HS induces inflammatory and hemodynamic changes in the kidney that are independent of SBP. Atorvastatin corrected all, suggesting that the nitric oxide-oxidative stress balance plays a significant role in the earlier stages of salt induced kidney damage.  
dc.format
application/pdf  
dc.language.iso
eng  
dc.publisher
American Physiological Society  
dc.rights
info:eu-repo/semantics/openAccess  
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/  
dc.subject
ATROVASTATIN  
dc.subject
BLOOD PRESSURE  
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KIDNEY INJURY  
dc.subject.classification
Patología  
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Medicina Básica  
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CIENCIAS MÉDICAS Y DE LA SALUD  
dc.title
Statins reverse renal inflammation and endothelial dysfunction induced by chronic high salt intake  
dc.type
info:eu-repo/semantics/article  
dc.type
info:ar-repo/semantics/artículo  
dc.type
info:eu-repo/semantics/publishedVersion  
dc.date.updated
2023-03-15T20:29:36Z  
dc.journal.volume
301  
dc.journal.number
2  
dc.journal.pagination
263-270  
dc.journal.pais
Estados Unidos  
dc.journal.ciudad
Bethesda  
dc.description.fil
Fil: Fiore, M. C.. No especifíca;  
dc.description.fil
Fil: Jimenez, P. M.. Universidad Nacional de San Luis; Argentina  
dc.description.fil
Fil: Cremonezzi, D.. Universidad Nacional de Córdoba; Argentina  
dc.description.fil
Fil: Juncos, L. I.. Instituto Privado de Investigaciones Médicas Mercedes y Martín Ferreyra; Argentina  
dc.description.fil
Fil: Garcia, Nestor Horacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina  
dc.journal.title
American Journal Of Physiology-renal Physiology  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://journals.physiology.org/doi/full/10.1152/ajprenal.00109.2010  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1152/ajprenal.00109.2010